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The Respiratory System Part 2

The Respiratory Cycle A respiratory cycle is a single cycle of inhalation and exhalation. The tidal volume is the amount of air you move into or out of your lungs during a single respiratory cycle.

The Mechanics of Breathing

The Respiratory Muscles

The most important are the diaphragm and the external intercostal muscles .

Muscles sed in !nhalation

!nhalation is an active process involving the contraction of one or more of these muscles"

The contraction of the diaphragm increases the volume of the thoracic cavity #y tensing and flattening its floor$ and this increase dra%s air into the lungs. &iaphragmatic contraction is responsi#le for roughly 75 percent of the air movement in normal #reathing at rest.

The external intercostal muscles assist in inhalation #y elevating the ribs. This action contri#utes roughly 2' percent to the volume of air in the lungs.

Accessory muscles$ including the sternocleidomastoid$ serratus anterior$ pectoralis minor$ and scalene muscles$ can assist the external intercostal muscles in elevating the ri#s. These muscles increase the speed and amount of ri# movement.

Muscles sed in (xhalation (xhalation is either passive or active$ depending on the level of respiratory activity. )hen exhalation is active$ it may involve one or more of the follo%ing muscles"

The internal intercostal and transversus thoracis muscles depress the ri#s and reduce the %idth and depth of the thoracic cavity.

The a#dominal muscles$ including the external and internal o#li*ue$ transversus a#dominis$ and rectus a#dominis muscles$ can assist the internal intercostal muscles in exhalation #y compressing the a#domen and forcing the diaphragm up%ard.

Respiratory Rates and +olumes

)hen you are exercising at pea, levels$ the amount of air moving into and out of the respiratory tract can #e 50 times the amount moved at rest.

Respiratory Rate is the num#er of #reaths you ta,e each minute. The normal respiratory rate of a resting adult ranges from -2 to -. #reaths each minute$ roughly one for every four heart#eats. Children #reathe more rapidly$ at rates of a#out -./20 #reaths per minute.

The Respiratory Minute +olume is the amount of air moved each minute$ sym#oli1ed #y multiplying the respiratory rate #y the tidal volume. This value is called the respiratory minute volume . The tidal volume at rest varies from individual to individual$ #ut it averages around 500 ml per breath. Therefore$ the respiratory minute volume at rest$ -2 #reaths per minute$ is approximately 2 liters per minute.

Alveolar +entilation

The volume of air in the conducting passages is ,no%n as the anatomic dead space.

Alveolar ventilation is the amount of air reaching the alveoli each minute. The alveolar ventilation is less than the respiratory minute volume$ #ecause some of the air never reaches the alveoli$ #ut remains in the dead space of the lungs.

At rest$ alveolar ventilation rates are approximately 3.2 liters per minute The gas arriving in the alveoli is different from that of the surrounding atmosphere$ #ecause inhaled air al%ays mixes %ith "used" air in the conducting passage%ays 4the anatomic dead space5 on its %ay to the exchange surfaces. The air in alveoli thus contains less oxygen and more car#on dioxide than atmospheric air.

Respiratory Performance and +olume Relationships Only a small proportion of the air in the lungs is exchanged during a single quiet respiratory cycle6 the tidal volume can #e increased #y inhaling more vigorously and exhaling more completely.

t Respiratory +olumes and Capacities. The resting tidal volume is the amount of air you move into or out of your lungs during a single respiratory cycle under resting conditions. The resting tidal volume averages a#out '00 ml in #oth males and females.

The expiratory reserve volume 4(R+5 is the amount of air that you can voluntarily expel after you have completed a normal$ *uiet respiratory cycle. As an example$ if$ %ith maximum use of the accessory muscles$ you can expel an additional -000 ml of air$ your expiratory reserve volume is -000 ml.

The residual volume is the amount of air that remains in your lungs even after a maximal exhalation/typically$ a#out -200 ml in males and --00 ml in females.

The minimal volume $ a component of the residual volume$ is the amount of air that %ould remain in your lungs if they %ere allo%ed to collapse. The minimal volume ranges from 70 to -20 ml$ #ut$ unli,e other volumes$ it cannot #e measured in a healthy person. 8ou %ould have to s*uee1e out the lungs li,e a sponge to measure it.

The inspiratory reserve volume 4!R+5 is the amount of air that you can ta,e in over and a#ove the tidal volume. !nspiratory reserve volumes differ significantly #y gender$ #ecause$ on average$ the lungs of males are larger than those of females. The inspiratory reserve volume of males averages 7700 ml$ compared %ith -900 ml in females.

)e can determine respiratory capacities #y adding the values of various volumes. (xamples include the follo%ing"

The inspiratory capacity is the amount of air that you can dra% into your lungs after you have completed a *uiet respiratory cycle. The inspiratory capacity is the sum of the tidal volume and the inspiratory reserve volume.

The functional residual capacity 4:RC5 is the amount of air remaining in your lungs after you have completed a *uiet respiratory cycle. The :RC is the sum of the expiratory reserve volume and the residual volume.

The vital capacity is the maximum amount of air that you can move into or out of your lungs in a single respiratory cycle. The vital capacity is the sum of the expiratory reserve$ the tidal volume$ and the inspiratory reserve and averages around 3.00 ml in males and 7300 ml in females.

The total lung capacity is the total volume of your lungs. The sum of the vital capacity and the residual volume$ the total lung capacity averages around 2000 ml in males and 3'00 ml in females.

;as (xchange

The actual process of gas exchange occurs #et%een #lood and alveolar air across the respiratory mem#rane. !t involves" 4-5 the partial pressures of the gases involved and 425 the diffusion of molecules #et%een a gas and a li*uid.

<xygen Transport (ach -00 ml of #lood leaving the alveolar capillaries carries a%ay roughly 20 ml of oxygen. <f this amount$ only a#out 0.7 ml 4-.' percent5 consists of oxygen molecules in solution. The rest of the oxygen molecules are #ound to hemoglo#in 4 =# 5 .

The percentage of heme units containing #ound oxygen at any given moment is called the hemoglo#in saturation .

The attachment of the first oxygen molecule ma,es it easier to #ind the second6 #inding the second promotes #inding of the third6 and #inding of the third enhances #inding of the fourth$ and so on.

At normal alveolar pressures the hemoglo#in saturation is very high 49>.' percent5$ although complete saturation does not occur until the reaches excessively high levels 4a#out 2'0 mm =g5.

!f the P?<2 increases$ the saturation goes up and hemoglo#in stores oxygen. !f the P?<2 decreases$ hemoglo#in releases oxygen into its surroundings .

)hen oxygenated #lood arrives in the peripheral capillaries$ the #lood P?<2 declines rapidly as a result of gas exchange %ith the interstitial fluid. As the P?<2 falls$ hemoglo#in gives up its oxygen.

Active tissues consume oxygen at an accelerated rate$ so the P?<2 may drop to -'/20 mm =g. =emoglo#in passing through these capillaries %ill then go from 9> percent saturation to a#out 20 percent saturation. This means that as #lood circulates through peripheral capillaries$ active tissues %ill receive 3.5 times as much oxygen as %ill inactive tissues.

Murder or suicide victims %ho died in their cars inside a closed garage are popular characters for mystery %riters. !n real life$ entire families are ,illed each %inter #y lea,y furnaces or space heaters. The cause of death is car#on monoxide poisoning . Car#on monoxide competes %ith oxygen molecules for the #inding sites on heme units. nfortunately$ the car#on monoxide usually %ins$ #ecause at very lo% partial pressures it has a much stronger affinity for hemoglo#in than does oxygen.

The #ond formed #et%een C< and heme is extremely durable$ so the attachment of a C< molecule essentially ma,es that heme unit inactive for respiratory purposes. Car#on monoxide %ill #ind to hemoglo#in at very lo% partial pressures. !f C< molecules ma,e up @ust 0.1 percent of the components of inhaled air$ enough hemoglo#in %ill #e affected that survival will become impossible %ithout medical assistance.

Treatment may include 4-5 the administration of pure oxygen in a hyper#aric cham#er$ #ecause at sufficiently high partial pressures$ the oxygen molecules %ill gradually replace C< at the hemoglo#in molecules$ and$ if necessary$ 425 the transfusion of compati#le red #lood cells.

=emoglo#in and p=

)hen the pH drops (more acidity)$ the shape of hemoglo#in molecules changes6 the oxygen saturation declines. Thus$ at a tissue of 30 mm =g$ hemoglo#in molecules release -' percent more oxygen at a p= of >.2 than they do at a p= of >.3. This effect of p= on the hemoglo#in saturation curve is called the Bohr effect . arbon dioxide is the primary compound responsi#le for the Bohr effect.

The (ffects of p= and Temperature on =emoglo#in Saturation. 4a5 )hen the p= drops #elo% normal levels$ more oxygen is released6 the hemoglo#in saturation curve shifts to the right. !f the p= increases$ less oxygen is released6 the curve shifts to the left. 4#5 )hen the temperature rises$ the saturation curve shifts to the right

=emoglo#in and Temperature

Changes in temperature also affect the slope of the hemoglo#in saturation curve . As the temperature rises$ hemoglo#in releases more oxygen6 as the temperature declines$ hemoglo#in

holds oxygen more tightly. :or example$ active s,eletal muscles generate heat$ and the heat %arms #lood that flo%s through these organs. As the #lood %arms$ the =# molecules release more oxygen than can #e used #y the active muscle fi#ers.

:etal =emoglo#in The RBCs of a developing fetus contain fetal hemoglo#in . The structure of fetal hemoglo#in$ %hich differs from that of adult hemoglo#in$ gives it a much higher affinity for oxygen. Also$ fetal hemoglo#in #inds more oxygen than does adult hemoglo#in

!daptations to High !ltitude

Atmospheric pressure decreases %ith increasing altitude$ and so do the partial pressures of the component gases$ including oxygen. People living in &enver or Mexico City function normally %ith alveolar oxygen pressures in the range of .0/90 mm =g. At higher elevations$ the alveolar partial pressures of oxygen continues to decline. At 7700 meters 4-0$.22 ft5$ an altitude familiar to many hi,ers and s,iers$ the alveolar P?<2 falls to around 20 mm =g.

Ppeople live and %or, at altitudes this high or higher. !mportant physiological ad@ustments include an increased respiratory rate" an increased heart rate" and an elevated hematocrit. Thus$ even though the hemoglo#in is not fully saturated$ the #loodstream holds more of it$ and the round/trip #et%een the lungs and the peripheral tissues ta,es less time. These responses represent an excellent example of the functional interplay #et%een the respiratory and cardiovascular systems. =o%ever$ most such adaptations ta,e days to %ee,s to appear. As a result$ athletes planning to compete in events held at high altitude must #egin training under such conditions %ell in advance.

Aot everyone can tolerate high/altitude conditions. Roughly 20 percent of people %ho ascend to 2200 meters 4.'70 ft5 or higher experience mountain sic,ness $ or altitude sic,ness . Symptoms may include headache$ disorientation$ and fatal pulmonary or cere#ral edema.

Car#on &ioxide Transport Car#on dioxide is generated #y aero#ic meta#olism in peripheral tissues. After entering the #loodstream$ a C<2 molecule is 4-5 converted to a molecule of car#onic acid$ 425 #ound to the protein portion of hemoglo#in molecules %ithin red #lood cells$ or 475 dissolved in plasma. All three are completely reversi#le reactions. Car#onic Acid :ormation Most of the car#on dioxide a#sor#ed #y #lood 4roughly >0 percent of the total5 is transported as molecules of carbonic acid. Car#on dioxide is converted to car#onic acid through the activity of the en1yme car#onic anhydrase in RBCs. The car#onic acid molecules immediately dissociate into a hydrogen ion and a bicarbonate ion.

Most of the hydrogen ions bind to hemoglobin molecules. The =# molecules thus function as buffers$ tying up the released hydrogen ions #efore the ions leave the RBCs and affect the plasma p=.

The #icar#onate ions move into the surrounding plasma %ith the aid of a countertransport mechanism that exchanges intracellular #icar#onate ions for extracellular chloride ions. This exchange$ %hich trades one anion for another$ does not re*uire ATP. The result is a mass movement of chloride ions into the RBCs$ an event ,no%n as the chloride shift .

=emoglo#in Binding Roughly 27 percent of the car#on dioxide carried #y your #lood %ill #e #ound to the glo#ular protein portions of the =# molecules inside RBCs. These molecules are attached to exposed amino groups of the =# molecules. The resulting compound is called car#aminohemoglo#in

Plasma Transport Plasma #ecomes saturated %ith car#on dioxide *uite rapidly$ and only a#out > percent of the car#on dioxide a#sor#ed #y peripheral capillaries is transported in the form of dissolved gas molecules.

Control of Respiration

The activities of the respiratory centers are coordinated with changes in cardiovascular function" such as fluctuations in blood pressure and cardiac output.

Bocal Regulation of ;as Transport and Alveolar :unction

<#viously$ if a peripheral tissue #ecomes more active$ the interstitial P?<2 falls and the P?C<2 rises.

Bocal factors coordinate 4-5 lung perfusion $ or #lood flo% to the alveoli$ %ith 425 alveolar ventilation $ or airflo%$ over a %ide range of conditions and activity levels.

As #lood flo%s toward the alveolar capillaries$ it is directed to%ard lo#ules in %hich the P?C<2 is relatively high.

This movement occurs #ecause alveolar capillaries constrict when the local #$ %& is lo%.

By directing #lood flo% to alveoli %ith lo% <2 levels and improving airflo% to alveoli %ith high C<2 levels$ local ad@ustments improve the efficiency of gas transport. These are local controls.

The Respiratory Centers of the Brain are three pairs of nuclei in the reticular formation of the medulla o#longata and pons. The motor neurons in the spinal cord are generally controlled #y respiratory reflexes $ #ut they can also #e controlled voluntarily through commands delivered #y the corticospinal path%ay.

Respiratory Centers in the Medulla <#longata

(ach center can #e su#divided into a dorsal respiratory group 4&R;5 and a ventral respiratory group 4+R;5 . The &R;Cs inspiratory center contains neurons that control lo%er motor neurons innervating the external intercostal muscles and the diaphragm. The &R; functions in every respiratory cycle$ %hether *uiet or forced.

'he ()* functions only during forced breathing.

There is reciprocal inhibition #et%een the neurons involved %ith inhalation and exhalation. )hen the inspiratory neurons are active$ the expiratory neurons are inhi#ited$ and vice versa. The pattern of interaction #et%een these groups differs #et%een *uiet #reathing and forced #reathing. &uring *uiet #reathing Activity in the &R; increases over a period of a#out 2 seconds$ providing stimulation to the inspiratory muscles. <ver this period$ inhalation occurs.

After 2 seconds$ the &R; neurons #ecome inactive. They remain *uiet for the next 7 seconds and allo% the inspiratory muscles to relax. <ver this period$ passive exhalation occurs. +o" you have about one breath per 5 seconds at rest.

&uring forced #reathing the level of activity in the &R; increases$ it stimulates neurons of the +R; that activate the accessory muscles involved in inhalation. At the end of each inhalation$ active exhalation occurs as the neurons of the expiratory center stimulate the appropriate accessory muscles

Basic Regulatory Patterns of Respiration. 4a5 Duiet #reathing.

4#5 :orced #reathing.

Central nervous system stimulants$ such as cocaine" amphetamines" ecstacy" or even caffeine$ increase your respiratory rate #y facilitating the respiratory centers. These actions can #e opposed #y CAS depressants$ such as ethyl alcohol" barbiturates or opiates. A mixture of these stimulants and depressants is often fatal.

The Apneustic and Pneumotaxic Centers The apneustic centers and the pneumotaxic centers of the pons are paired nuclei that ad@ust the output of the respiratory rhythmicity centers. Their activities regulate the respiratory rate and the depth of respiration in response to sensory stimuli or input from other centers in the #rain.

(ach apneustic center provides continuous stimulation to the &R; on that side of the #rain stem. &uring *uiet #reathing$ stimulation from the apneustic center helps increase the intensity of inhalation over the next 2 seconds. nder normal conditions$ after 2 seconds the apneustic center is inhi#ited #y signals from the pneumotaxic center on that side. &uring forced #reathing$ the apneustic centers also respond to sensory input from the vagus nerves regarding the amount of lung inflation. The pneumotaxic centers inhi#it the apneustic centers and promote passive or active exhalation. Centers in the hypothalamus and cere#rum can alter the activity of the pneumotaxic centers$ as %ell as the respiratory rate and depth. =o%ever$ essentially normal respiratory cycles continue even if the #rain stem superior to the pons has #een severely damaged. !f the inhi#itory output of the pneumotaxic centers is cut off #y a stro,e or other damage to the brain stem$ and if sensory innervation from the lungs is eliminated #y cutting the vagus nerves$ the person inhales to maximum capacity and maintains that state for 10-&0 seconds at a time. .ntervening exhalations are brief" and little pulmonary ventilation occurs.

Pathways for conscious control over respiratory muscles are not shown.

Respiratory Reflexes The activities of the respiratory centers are modified #y sensory information from several sources" -. Chemoreceptors sensitive to the p=$ or of the #lood or cere#rospinal fluid.

2. Changes in #lood pressure in the aortic or carotid sinuses. 7. Stretch receptors that respond to changes in the volume of the lungs. 3. !rritating physical or chemical stimuli in the nasal cavity$ larynx$ or #ronchial tree. '. <ther sensations$ including pain$ changes in #ody temperature$ and a#normal visceral sensations. !nformation from these receptors alters the pattern of respiration. The induced changes have #een called respiratory reflexes .

Sudden infant death syndrome 4S!&S5 $ also ,no%n as cri# death $ ,ills an estimated -0$000 infants each year in the nited States alone 4the %orld?%ide #irth rate is one every > seconds5. Most cri# deaths occur #et%een midnight and 9"00 A.M.$ in the late fall or %inter$ and involve infants t%o to four months old.

The age at the time of death corresponds %ith a period %hen the pacema,er complex and respiratory centers are establishing connections with other portions of the brain. !t has recently #een proposed that S!&S results from a pro#lem in the interconnection process that disrupts the reflexive respiratory pattern.

The Chemoreceptor Reflexes The respiratory centers are strongly influenced #y chemoreceptor inputs from cranial nerves !E and E and from receptors that monitor the composition of the cere#rospinal fluid 4CS:5"

Chemoreceptors are located on the ventrolateral surface of the medulla o#longata in a region ,no%n as the chemosensitive area . The neurons in that area respond only to the and p= of the CS: and are often called central chemoreceptors .

The Baroreceptor Reflexes )e descri#ed the effects of carotid and aortic #aroreceptor stimulation on systemic #lood pressure in Chapter 2- . The output from these #aroreceptors also affects the respiratory centers. )hen #lood pressure falls$ the respiratory rate increases6 %hen #lood pressure rises$ the

respiratory rate declines. This ad@ustment results from the stimulation or inhi#ition of the respiratory centers #y sensory fi#ers in the glossopharyngeal 4!E5 and vagus 4E5 nerves.

Protective Reflexes operate %hen you are exposed to toxic vapors$ chemical irritants$ or mechanical stimulation of the respiratory tract. The receptors involved are located in the epithelium of the respiratory tract. (xamples of protective reflexes include snee1ing$ coughing$ and laryngeal spasms.

Snee1ing is triggered #y an irritation of the %all of your nasal cavity. Coughing is triggered #y an irritation of your larynx$ trachea$ or #ronchi. Both reflexes involve apnea$ a period in %hich respiration is suspended. They are usually follo%ed #y a forceful expulsion of air intended to remove the offending stimulus. The glottis is forci#ly closed %hile the lungs are still relatively full. The a#dominal and internal intercostal muscles then contract suddenly$ creating pressures that %ill #last air out of your respiratory passage%ays %hen the glottis reopens. !ir leaving the larynx can travel at 160 ph !"" mph#" carrying mucus" foreign particles" and irritating gases out of the respiratory tract via the nose or mouth.

Baryngeal spasms result from the entry of chemical irritants$ foreign o#@ects$ or fluids into the area around the glottis. This reflex generally closes your air%ay temporarily. A very strong stimulus$ such as a toxic gas$ could close the glottis so po%erfully that you could lose consciousness and die %ithout ta,ing another #reath. :ine chic,en #ones or fish #ones that pierce the laryngeal %alls can also stimulate laryngeal spasms$ s%elling$ or #oth$ restricting the air%ay.

<ther Sensations That Affect Respiratory :unction Several other sensory stimuli can affect the activities of the respiratory centers. (xamples include the follo%ing"

Sudden pain or immersion in cold %ater can produce a temporary apnea.

Chronic pain stimulates the sympathetic division of the autonomic nervous system$ leading to an increase in the respiratory rate.

Both fever and an increase in #ody temperature due to exertion or overheating cause an increase in the respiratory rate. A reduction in #ody temperature leads to a decrease in the respiratory rate.

Curiously$ stretching the anal sphincter stimulates the respiratory centers and increases the rate of respiration. Although this reflex is occasionally used to stimulate respiration in an emergency$ it is not clear %hich path%ays are involved. $nough said a%out that&

+oluntary Control of Respiration Activity of your cere#ral cortex has an indirect effect on your respiratory centers$ as the follo%ing examples sho%"

Conscious thought processes tied to strong emotions$ such as rage or fear$ affect the respiratory rate #y stimulating centers in the hypothalamus.

(motional states can affect respiration through the activation of the sympathetic or parasympathetic division of the autonomic nervous system. Sympathetic activation causes #ronchodilation and increases the respiratory rate6 parasympathetic stimulation has the opposite effect.

An anticipation of strenuous exercise can trigger an automatic increase in the respiratory rate$ along %ith increased cardiac output$ #y sympathetic stimulation.

8ou cannot ,ill yourself #y holding your #reath Ftill you turn #lue.F <nce the rises to critical levels$ you %ill #e forced to ta,e a #reath.

Changes in the Respiratory System at Birth

Before delivery$ pulmonary arterial resistance is high$ #ecause the pulmonary vessels are collapsed. The ri# cage is compressed$ and the lungs and conducting passage%ays contain only small amounts of fluid and no air. &uring delivery$ the lungs are compressed further$ and as the

placental connection is lost$ #lood oxygen levels fall and car#on dioxide levels clim# rapidly. At #irth$ the ne%#orn infant ta,es a truly heroic first #reath through po%erful contractions of the diaphragmatic and external intercostal muscles.

The changes in #lood flo% that occur lead to the closure of the foramen ovale $ an interatrial connection$ and the ductus arteriosus $ the fetal connection #et%een the pulmonary trun, and the aorta.

Su#se*uent #reaths complete the inflation of the alveoli.

Aging and The Respiratory System

Many factors interact to reduce the efficiency of the respiratory system in elderly individuals. Three examples are particularly note%orthy"

As oneCs age increases$ elastic tissue deteriorates throughout the body$ reducing the compliance of the lungs and lo%ering their vital capacity.

Chest movements are restricted by arthritic changes in the rib articulations and by decreased flexibility at the costal cartilages. The stiffening and reduction in chest movement effectively limit the respiratory minute volume. This restriction contri#utes to the reduction in exercise performance and capa#ilities %ith increasing age.

Some degree of emphysema is normal in individuals over age '0. =o%ever$ the extent varies %idely %ith the lifetime exposure to cigarette smo,e and other respiratory irritants.

/mphysema $ 0ung ancer

(mphysema is a chronic$ progressive condition characteri1ed #y shortness of #reath and an ina#ility to tolerate physical exertion. The underlying pro#lem is the destruction of alveolar surfaces and inadequate surface area for oxygen and car%on dioxide exchange. !n essence$ respiratory #ronchioles and alveoli are functionally eliminated.

(mphysema has #een lin,ed to the inhalation of air that contains fine particulate matter or toxic vapors$ such as those in cigarette smo,e.

An estimated 22 percent of adult males and 2' percent of adult females have detecta#le areas of emphysema in their lungs.

Bung cancer is an aggressive class of malignancies originating in the bronchial passageways or alveoli. These cancers affect the epithelial cells that line conducting passage%ays$ mucous glands$ or alveoli. Symptoms generally do not appear until the condition has progressed to the point at %hich the tumor masses are restricting airflo% or compressing ad@acent structures

&eaths from lung cancer %ere rare at the turn of the 20th century$ #ut 29$000 such deaths occurred in -9'2$ -0'$000 in -9>.$ and -'3$900 in 2002 in the nited States. This rise coincides %ith an increased rate of smo,ing in the population.

Bung cancer is increasing mar,edly among %omen$ #ut declining among men.

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